Increased activity of CaMKII [which may occur due to CaMKII overexpression (Zhang et al., 2002, 2003) or upregulation in the failing heart (Anderson, 2005)] alters Ca2+ homeostasis [including increased Ca2+ entry through ICaL (Anderson et al., 1994); increased Ca2+ release through RyR (Wehrens et al., 2004); and increased Ca2+ reuptake to the SR (Mattiazzi and Kranias, 2014)] and enhances the late sodium current (INaL) (Wagner et al., 2006; Maltsev et al., 2008), both effects promoting abnormal cellular triggered activity and arrhythmia (Anderson, 2005; Vincent et al., 2014). This evidence concerns the gene CAMK2G and cardiac arrhythmia.